Study Finds Benefit to Interventional Reduction Chemotherapy for Patients With AML
Posted: Monday, August 9, 2021
For patients with relapsed or refractory acute myeloid leukemia (AML), intensive reduction chemotherapy should be implemented as the primary therapeutic intervention to achieve complete remission, according to a preliminary study published in the International Journal of Cancer. This strategy improves patient prognosis and allows the use of allogeneic hematopoietic stem cell transplantation (allo-HSCT) as a supplemental treatment, explained Donghua Zhang, MD, PhD, of Tongji Hospital, China, and colleagues.
The clinical and survival data of 112 patients with relapsed or refractory AML were recruited for the study. Patients were either treated with conventional regimens (n = 102) or with a treatment regimen that included decitabine, cladribine, idarubicin or homoharringtonine, and cytarabine (DCIA/DCHA; n = 10). Reverse-transcriptase polymerase chain reaction was performed to evaluate molecular differences, whereas G-banding analysis was used to assess cytogenic differences. Based on patients’ response to the first chemotherapy session, they were subdivided into those who achieved complete remission (n = 40) and those who did not (n = 62).
The study authors reported that those patients who had greater than 70% of bone marrow blasts and could not achieve complete remission following the first reinduction chemotherapy session had a poorer overall prognosis. In contrast, patients who received allo-HSCT after achieving complete remission experienced improvement in overall prognosis. In addition, 90% of patients who received DCIA/DCHA therapy achieved complete remission despite incomplete hematopoietic recovery after their first chemotherapy treatment. Moreover, the study findings revealed a 10.14-month overall median survival for patients who received DCIA/DCHA treatment. However, all these patients demonstrated grade 4 myelosuppression.
Disclosure: For full disclosures of the study authors, visit onlinelibrary.wiley.com.